ArticleCell death discovery2024
Parthanatos initiated by ROS-induced DNA damage is involved in intestinal epithelial injury during necrotizing enterocolitis.
Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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Who cites it
14 citing papers in PubMed.
- Elucidating shared genes and pathways in programmed cell death with necrotizing enterocolitis: insights into novel therapeutic targets and glutathione.Translational pediatrics · 2026Article
- Navigating a thorny path: oral nanomedicines for the precision management of radiation-induced intestinal injury.Journal of nanobiotechnology · 2026Review
- LncRNA DANCR Regulates PARP1-Mediated Oxidative Stress Response in Corneas by Encoding a Novel Micropeptide miPEPDR.Investigative ophthalmology & visual science · 2026Article
- Exploration of Carotenoid-Producing Microorganisms from the Kuril-Kamchatka Trench and Their Antioxidant Potential.Marine drugs · 2026Article
- Reactive oxygen species (ROS) in cancer: from redox signaling and metabolic plasticity to therapeutic vulnerabilities.Exploration of targeted anti-tumor therapy · 2026Review
- Ferroptosis in necrotizing enterocolitis: iron overload-driven intestinal injury and mechanistic insights.Frontiers in pediatrics · 2026Review
- Screening and Preliminary Validation of Parthanatos-Related Key Genes in Asthma Using Transcriptomic and Machine Learning Approaches.Journal of inflammation research · 2026Article
- High-Altitude Hypoxia Injury: Systemic Mechanisms and Intervention Strategies on Immune and Inflammatory Responses.Antioxidants (Basel, Switzerland) · 2025Review
- METTL3-dependent mAutophagy · 2025Article
- Identification of potential necroinflammation-associated necroptosis-related biomarkers in necrotizing enterocolitis based on bioinformatics analysis and machine learning.Translational pediatrics · 2025Article
- PJ34 prevents cisplatin-induced hair cell loss via inhibition of PARP-1-AIF parthanatos.Biomolecules & biomedicine · 2025Article
- Advances in non-apoptotic regulated cell death: implications for malignant tumor treatment.Frontiers in oncology · 2025Review
- Temporal transcriptomic atlas reveals sequential engagement of classical and emerging regulated cell death pathways during PRRSV infection.Frontiers in veterinary science · 2025Article
- Parthanatos and apoptosis: unraveling their roles in cancer cell death and therapy resistance.EXCLI journal · 2025Review
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Necrotizing enterocolitis (NEC) involves intestinal epithelial damage and inflammatory response and is associated with high morbidity and mortality in infants. To improve therapeutic prospects, elucidating underlying molecular mechanisms of intestinal epithelial damage during NEC is of the essence. Poly (ADP-ribose) polymerase 1 (PARP1)-dependent parthanatos is a programmed inflammatory cell death. In the present study, the presence of parthanatos-associated proteins PARP1 and poly (ADP-ribose) (PAR), along with high expression of DNA damage-associated biomarkers, 8-hydroxy-2'-deoxyguanosine (8-OHdG) and phosphorylation of histone H2AX (γH2AX), were discovered in the intestinal tissues of NEC infants. Additionally, the upregulated expression of PARP1 and PAR in NEC intestinal tissues correlated distinctly with clinical indices indicative of NEC incidence and severity. Furthermore, we demonstrated that inhibiting the expression of parthanatos-associated proteins, by either pharmacological blockage using 3-aminobenzamide (3-AB), an inhibitor of PARP1, or genetic knockout using Parp1-deficient mice, resulted in substantial improvements in both histopathological severity scores associated with intestinal injury and inflammatory reactions. Moreover, in an in vitro NEC model, reactive oxygen species (ROS)-induced DNA damage promoted the formation of PAR and nuclear translocation of apoptosis-inducing factor (AIF), thus activating PARP1-dependent parthanatos in Caco-2 cells and human intestinal organoids. Our work verifies a previously unexplored role for parthanatos in intestinal epithelial damage during NEC and suggests that inhibition of parthanatos may serve as a potential therapeutic strategy for intervention of NEC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.